ArticleAmerican journal of physiology. Cell physiology2014
Heart failure-induced changes of voltage-gated Ca2+ channels and cell excitability in rat cardiac postganglionic neurons.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Systemic Neutralization of Granulocyte-Macrophage Colony-Stimulating Factor Attenuates Stellate Ganglion Neuroinflammation and Cardiac Sympathetic Overactivation in Chronic Heart Failure in Rats.International journal of molecular sciences · 2026Article
- Article
- The Heart's Hidden Neural Network: Interplay Between Intracardiac Ganglia, Fibrosis and Cardiac Remodeling.International journal of molecular sciences · 2026Review
- Impact of PKC-MAPK Signaling on Cardiac Sympathetic Overactivation in Type-2 Diabetes Mellitus.International journal of molecular sciences · 2026Article
- Role of Cav1.3 Channels in Brain-Heart Interactions: An Unexpected Journey.Biomedicines · 2025Review
- Hydrogen Peroxide-Induced Re-Expression of Repressor Element 1-Silencing Transcription Factor Contributes to Cardiac Vagal Dysfunction in Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2025Article
- Stellate Ganglia: A Key Therapeutic Target for Malignant Ventricular Arrhythmia in Heart Disease.Circulation research · 2025Review
- Bayliss Starling Prize Lecture 2023: Neuropeptide-Y being 'unsympathetic' to the broken hearted.The Journal of physiology · 2025Article
- Age-dependent reduction in voltage-gated inward sodium current and Scn8a gene expression in murine stellate ganglia.Annals of the New York Academy of Sciences · 2025Article
- Cellular and Molecular Mechanisms Underlying Altered Excitability of Cardiac Efferent Neurons in Cirrhotic Rats.Biomedicines · 2024Article
- Identification and verification of feature biomarkers associated in heart failure by bioinformatics analysis.Scientific reports · 2023Article
- Recording plasticity in neuronal activity in the rodent intrinsic cardiac nervous system using calcium imaging techniques.Frontiers in synaptic neuroscience · 2023Article
- Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022Review
- Hydrogen Peroxide Scavenging Restores N-Type Calcium Channels in Cardiac Vagal Postganglionic Neurons and Mitigates Myocardial Infarction-Evoked Ventricular Arrhythmias in Type 2 Diabetes Mellitus.Frontiers in cardiovascular medicine · 2022Article
- Vagally-mediated heart block after myocardial infarction associated with plasticity of epicardial neurons controlling the atrioventricular node.Frontiers in synaptic neuroscience · 2022Article
- Macrophage depletion in stellate ganglia alleviates cardiac sympathetic overactivation and ventricular arrhythmogenesis by attenuating neuroinflammation in heart failure.Basic research in cardiology · 2021Article
- Reduced Cell Excitability of Cardiac Postganglionic Parasympathetic Neurons Correlates With Myocardial Infarction-Induced Fatal Ventricular Arrhythmias in Type 2 Diabetes Mellitus.Frontiers in neuroscience · 2021Article
- Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure.Cardiovascular research · 2021Article
- Novel approaches to restore parasympathetic activity to the heart in cardiorespiratory diseases.American journal of physiology. Heart and circulatory physiology · 2020Review
- Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches.The Journal of physiology · 2020Review
Corrections and comments
- Commented on by
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic heart failure (CHF) is characterized by decreased cardiac parasympathetic and increased cardiac sympathetic nerve activity. This autonomic imbalance increases the risk of arrhythmias and sudden death in patients with CHF. We hypothesized that the molecular and cellular alterations of cardiac postganglionic parasympathetic (CPP) neurons located in the intracardiac ganglia and sympathetic (CPS) neurons located in the stellate ganglia (SG) possibly link to the cardiac autonomic imbalance in CHF. Rat CHF was induced by left coronary artery ligation. Single-cell real-time PCR and immunofluorescent data showed that L (Ca(v)1.2 and Ca(v)1.3), P/Q (Ca(v)2.1), N (Ca(v)2.2), and R (Ca(v)2.3) types of Ca2+ channels were expressed in CPP and CPS neurons, but CHF decreased the mRNA and protein expression of only the N-type Ca2+ channels in CPP neurons, and it did not affect mRNA and protein expression of all Ca2+ channel subtypes in the CPS neurons. Patch-clamp recording confirmed that CHF reduced N-type Ca2+ currents and cell excitability in the CPP neurons and enhanced N-type Ca2+ currents and cell excitability in the CPS neurons. N-type Ca2+ channel blocker (1 μM ω-conotoxin GVIA) lowered Ca2+ currents and cell excitability in the CPP and CPS neurons from sham-operated and CHF rats. These results suggest that CHF reduces the N-type Ca2+ channel currents and cell excitability in the CPP neurons and enhances the N-type Ca2+ currents and cell excitability in the CPS neurons, which may contribute to the cardiac autonomic imbalance in CHF.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.